• Medication methods of treatment
  • Chemotherapy of disseminated pancreatic cancer in monotherapy regimen
    • Fluorouracil.

      Fluorouracil (FU) is a synthetic analogue of the naturally occurring pyrimidine - uracil. The main target is the enzyme thymidylate synthetase, which controls the synthesis of normal thymidine nucleotides. During infusion, the Fluorouracil solution must be protected from light. Patients are advised not to use aspirin and other non-steroidal anti-inflammatory drugs together with Fluorouracil.

      The drug is used in different modes:

      • 500 mg / m 2 IV stream for 5 consecutive days, every 4 weeks or
      • 500-600 mg / m 2 IV, jet 1 time per week, 6 weeks or
      • 1000 mg / m 2 IV infusion for 5 days (120 hours) every 4 weeks or
      • 200-300 mg / m 2 IV, by infusion for a month or
      • 2.6 g / m 2 intravenously, by infusion over 24 hours, once a week, 4-5 weeks.
    • Mitomycin C (MMS).

      MMC is an antibiotic in origin; in terms of its mechanism of action, it refers to alkylating agents that require activation in vivo. Among side effects MMS - leukopenia and especially thrombocytopenia. Rarely, the drug causes the development of interstitial pneumonia, when used together with anthracyclines, it increases the cardiotoxicity of the latter.

      The drug is administered intravenously. It is prescribed at 10-20 mg / m 2 every 6-8 weeks, or 5-6 mg / m 2 every 4 weeks.

    • Streptozocin (Szt).

      By chemical structure the drug belongs to nitrosoureas with a D-glucopyranose bond. By its mechanism of action, Szt is a typical DNA alkylator. It enters the cells of the islet apparatus and this explains its antitumor activity in neoplasms of the endocrine pancreas.

      The drug is administered strictly intravenously at 500 mg / m 2 for 5 days every 6 weeks.

      Complications include renal toxicity, vomiting, moderate myelosuppression, hypoglycemia, fever, depression, and lethargy.

    • Semustin or Methyl Nitrosourea (Methyl CCNU).

      Belongs to the class of nitrosoureas. It is an alkylating agent. In pancreatic cancer, the drug is effective in 13% of cases.

    • Doxorubicin (ADM).

      An antibiotic from the anthracyclines group, consisting of a multi-ring chromophore and an amino sugar. The main mechanism of ADM action is the intercalation of the chromophore between DNA strands. In addition, the enzyme topoisomerase II, which is responsible for the topology of DNA, is suppressed and free radicals are generated, which are cytotoxic to tumor and normal tissues.

      ADM is given IV or intra-arterially. It is prescribed in doses of 25-30 mg / m 2 2 days every 3-4 weeks, or 20 mg / m 2 weekly, or 60-75 mg / m 2 1 time in 3 weeks.

      Cardiotoxicity is considered the most serious complication.

    • Epirubicin (EPI).

      It is a stereoisomer of doxorubicin, differs from it in the orientation of the hydroxyl group at the 4 position in the amino sugar. The antitumor effect is recorded in the range of 13-37%. The annual survival rate is 12%.

      It is used in doses of 75-90 mg / m 2 every 21 days. The drug is administered strictly intravenously. The total dose should not exceed 700 mg / m 2.

      Common complications include myelosuppression, mucositis, nausea and vomiting. Among the rare side effects are increased uric acid, thrombocytopenia, phlebosclerosis, diarrhea, dark spots on the skin, nail changes, allergic reactions.

    • Ifosfamide (IFO).

      Refers to chloroethylamines, is a synthetic analogue of cyclophosphamide. It is activated in the liver by microsomal enzymes. Its active metabolite, 4-hydroxyphosphamide, alkylates DNA, causing it to break, as well as RNA, and inhibits protein synthesis.

      Complications are observed: myelosuppression, nausea, vomiting, diarrhea and sometimes constipation, alopecia, hepatotoxicity, rarely lethargy, hallucinations; symptoms of cystitis may occur - dysuria, frequent urination.

      The most common modes (I / O):

      • 1000 mg / m 2 5 consecutive days every 3 weeks or
      • 1.2-2.4 g / m2 3 consecutive days every 3 weeks or
      • 5000 mg / m 2 1 time in 3 weeks.
    • Tomudex (Raltitrexed).

      Quinazoline antifolate is a direct and specific inhibitor of thymidylate synthetase. After entering the tumor cell, the drug is polyglutaminated by the action of folipolyglutamate synthetase. Tomudex is active in monotherapy in 12-14% of cases. Stabilization of tumor growth is observed in 29% of patients.

      Introduced at 3 mg / m 2 / in 1 time in 3 weeks.

      Among the complications: leukopenia (18%), diarrhea (10%), mucositis (3%), asthenia (18%), vomiting (13%), increased transaminases (7%).

    • UFT.

      UFT is a formulation of fluoroafur and uracil. The molar ratio of these components is 1: 4. The effectiveness of the drug is recorded in 22.7% of cases.

    • UDR (floxouridine).

      This synthetic analogue of deoxyuridine is a metabolite of fluorouracil.

      The drug is administered intravenously or intraarterially. When administered intravenously, the FUDR dose is 0.1-0.15 mg / kg per day for 14 days; the cycles are repeated every 4 weeks. When administered intra-arterially, the FUDR dose is 0.2-0.3 mg / kg per day, 14 days; the cycles are repeated every 4 weeks.

      Complications of FUDR are: nausea, vomiting, mucositis, diarrhea (29%), gastritis, headache, itching, dermatitis, increased transaminases.

    • Irinotecan or Campto (Cpt-11).

      Refers to inhibitors of topoisomerase I. It is analogous to camptothecin.

      It is administered intravenously, at a dose of 350 mg / m 2 once every 3 weeks (5-6 doses).

      Complications include diarrhea, neutropenia, sometimes with fever, vomiting, allergic reactions, stomatitis.

      In pancreatic cancer, it is effective in 12% of patients.

    • Paclitaxel (Tax).

      It is a complex diterpene with a taxane ring and a carbohydrate chain (essential for anti-tumor activity). Paclitaxel is of vegetable origin, isolated from the bark of the California yew. Tax - (the first active drug from the group of taxanes) stimulates the chaotic and irregular formation of microtubules from tubulin and then prevents their breakdown. These skeletal disorders of tumor cells lead to their death. Stabilization of the tumor process was noted in 20% of Tax.

      Tax is administered in doses of 175-200 mg / m2 intravenously, by infusion, within 3 hours (sometimes 24) 1 time in 3 weeks with preliminary premedication.

      Side effects include myelosuppression, anemia and thrombocytopenia, pressure drop (12%), neurotoxicity (60%), anorexia, alopecia, vomiting, and mucositis are not common.

    • Docetaxel or Taxotere (Tht).

      The mechanism of action of the drug lies in the destruction of the cell skeleton due to the stimulation of the formation of microtubules and the suppression of their depolymerization.

      Txt is used intravenously in doses of 100 mg / m 2 once every 3 weeks (5-6 cycles). Premedication with diphenhydramine and steroids is also required to reduce hypersensitivity.

      Side effects are observed: neutropenia (70%), dermatological toxicity (60%), fluid retention (30-68%), diarrhea (31%), stomatitis (20%), neurotoxicity (12%), other complications are rare.

    • Gemcitabine or Gemzar (Gem).

      Gem is a fluorine-substituted analogue of deoxycytidine, structurally similar to cytosar. However, unlike the latter, it is more lipophilic and, as a result, passes faster through the membrane of tumor cells. It has a greater affinity for the target - deoxycidine kinase; its active metabolite gemcitabine triphosphate is longer than the cytosar is in the tumor cell.

      Gemzar is applied intravenously at 1000 mg / m 2 in 1,8,15 days, every 4 weeks. Among the complications from Gem use: leukopenia (19%), thrombocytopenia (22%), asthenia (12%), peripheral edema (10%).

    • Erlotinib (Tarceva).

      Erlotinib (Tarceva) is a reversible and highly specific inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase. Tyrosine kinase is responsible for the intracellular phosphorylation of HER1 / EGFR. HER1 / EGFR expression is observed on the surface of both normal and tumor cells. Inhibition of phosphotyrosine by EGFR inhibits the growth of tumor cell lines and / or leads to their death.

      For pancreatic cancer, 100 mg is used daily, for a long time, in combination with gemcitabine.

  • Combined chemotherapy for unresectable pancreatic cancer

    Over the past decades, various combinations of chemotherapy drugs have been used to treat pancreatic cancer.

    • Fluorouracil-based combinations.
      • FAM combination.

        The combination consists of fluorouracil administered at 600 mg / m 2 IV 1 time per week for 1,2,5,6 and 9 weeks; doxorubicin, used at 30 mg / m 2 once a week for 1.5 and 9 weeks; mitomycin C, applied at 10 mg / m 2 once a week for 1 and 9 weeks.

      • Combination SMF.

        The combination differs from FAM by replacing doxorubicin with streptozotocin.

        2 types of SMF were used:

        • SMF1 (streptozotocin 1 g / m2 IV, once a week, at 1, 2, 5, 6 and 9 weeks; mitomycin C 10 mg / m2 IV once a week at 1, 6 and 9 weeks, fluorouracil 600 mg / m 2 once a week at 1, 2, 5, 6 and 9 weeks).
        • SMF2 (streptozotocin 350 mg / m 2 once a week, at 1-5 and 9 weeks; mitomycin C 10 mg / m 2 once a week at 1 and 9 weeks; fluorouracil 600 mg / m 2 once per week 1-5 and 9th weeks).
      • MFL mode.

        Mitomycin C 12 mg / m 2 day 1, fluorouracil 400 mg / m 2 days 1-5 and leucovorin 200 mg / m 2 days 1-5. The regimen is applied every 4 weeks.

      • Combination EVFL.

        Consists of epirubicin (60 mg / m 2 day 1), etoposide (80 mg / m 2 intravenously 1-3 days), fluorouracil (340 mg / m 2 1-3 days) and leucovorin (100 mg / m 2 intravenously 1 - 3 days). The antitumor effect was registered in 15% of patients.

    • Combinations based on cisplatin.
      • FAP combination. Consists of fluorouracil, doxorubicin and cisplatin.
      • The FP combination includes fluorouracil (1 g / m 2 iv on days 1-5) and cisplatin (100 mg / m 2 on the 2nd day). The cycles are repeated every 4 weeks. The effect was registered in 26% of patients.
      • The CAC combination consists of cisplatin, cytosar and caffeine. Achieved The effect is achieved in 39% of cases.
    • Combinations using gemcitabine (gemzar).
      • Gemzar (1000 mg / m 2 1,8,15 days) is combined with fluorouracil infusion (200 mg / m 2 1-5 days).
      • The combination of gemzar + fluorouracil + leucovorin. The recommended Gem regimen is 1000 mg / m2 i / v 1,8,15 days; FU 500 mg / m 2 1-5 days; FA 20 mg / m 2 1-5 days.

• Radiation therapy

  Treatment is carried out preoperatively, intraoperatively, postoperatively, in combination with chemotherapy.

  Radiation therapy for patients with pancreatic cancer uses different doses of radiation.

  For palliative purposes (pain control, jaundice, prevention of bleeding), the radiation dose is 50 Gy. Higher doses of more than 60 Gy are prescribed to patients in order to improve survival rates.

  Preoperative radiation is rarely used.

  Intraoperative radiation can be combined with external radiation in order to increase the dose to the pancreas and provide better local control of the disease. The intraoperative radiation dose varies from 10 to 20 Gy; external - from 45 to 50 Gy. Remission within a year is observed in 82% of patients.

• Chemoradiation treatment for pancreatic cancer

  One of the ways to improve the results in inoperable pancreatic cancer is the combination of radiation therapy and promising anticancer drugs.

  • Radiation therapy and gemzar.
    • 20 fractions of external irradiation (dose 35 Gy) with a 2-week break after 10 fractions. Gemzar in a dose of 400 mg / m 2 is prescribed 2 times a week for 1-3 and 5-7 weeks.
    • Gemzar at a dose of 1000 mg / m2 on days 1,8,15 of external radiation therapy (dose 27 Gy, 15 fractions).
  • Radiation therapy and fluorouracil.
    • A combination of radiation therapy (60Gy) + (FAP) fluorouracil + doxorubicin + cisplatin.
    • A combination of FEP (fluorouracil 200 mg / m 2 - continuous infusion + epirubicin 50 mg / m 2 and cisplatin 60 mg / m 2 once every 3 weeks together with conformal irradiation (63 Gy for 6 weeks).
  • Other combinations.

    Radiation therapy (45 Gy) is combined with UFT (150-300 mg per day) and leucovorin (90 mg per day).

• Neoadjuvant and Adjuvant Therapy for Pancreatic Cancer

  Adjuvant therapy (surgery and postoperative chemoradiation therapy) is one of the options for treating pancreatic cancer. However, less than 20% of patients are operable by the time of initial diagnosis, therefore, the maximum result from adjuvant treatment can be obtained only in 4% of the total number of patients.

  A neoadjuvant approach to the treatment of locally advanced pancreatic cancer makes it possible to increase the percentage of resectable tumors up to 40% (20% due to potentially resectable patients and 20% due to unresectable patients at the time of initial diagnosis by restaging) and lengthen the life of patients.

  As part of the neoadjuvant approach, chemoradiotherapy can be used before surgery. In some cases, preoperative radiation therapy is performed followed by intraoperative radiation. This type of therapy increases patient survival to 2 years in 27% of cases; up to 5 years - in 7% of cases.

  The use of chemotherapy alone as a neoadjuvant treatment does not lead to a significant increase in survival rates.

• Palliative care
  • Relief of pain syndrome.
    • For this purpose, narcotic analgesics are used in combination with tricyclic antidepressants or anti-memetic drugs (which can also potentiate the action of analgesics).
    • Celiac ganglia neurolysis can lead to a decrease in pain intensity. The procedure is carried out transthoracally, transabdominally, transgastrically or during surgery.
    • Radiotherapy also contributes to the partial relief of pain.
  • Elimination of jaundice.
    • With the appearance of obstructive jaundice, patients begin to be bothered by itching, pain in the right upper quadrant of the abdomen (worse after eating), or they develop cholangitis.
    • If patients have obstruction of the pancreatic duct (in 5% of cases) or biliary tract, then they undergo endoscopic decompression with stenting.
    • Endoscopic decompression with stenting is performed during choledochojejunostomy, cholecystojejunostomy, gastrojejunostomy, or when performing resection of a pancreatic tumor. For these purposes, metal and plastic stents are used (they must be changed every 3-4 months).
    • If the results of the procedure are unsatisfactory, then the patients are prescribed: cholestyramine (Questran) inside, 4 g 1-4 r / day; phenobarbital (Luminal) inside, 30-60 mg 2-4 r / day.
  • Treatment of disorders of the exocrine function of the pancreas.

    Enzyme preparations are prescribed (for example, Creon).

• Surgery

  Surgical treatment is performed in the absence of distant metastases and radiographic or clinical signs of tumor unresectability.

  Preoperative concepts of tumor resectability are preliminary. The final decision is made after an intraoperative examination of the organs. abdominal cavity (liver, peritoneum, periaortic and celiac lymph nodes) to exclude distant metastases. Then the possibilities of local tumor resectability are determined.

  Pancreatoduodenal resection (Whipple operation) is the main type of radical surgery. It is not performed if the tumor invades the inferior vena cava, aorta, superior mesenteric artery, superior mesenteric vein, portal vein. To decide on the operation, it is necessary to mobilize the duodenum and the head of the pancreas from the underlying inferior vena cava and aorta. This technique also allows one to judge the involvement of the superior mesenteric artery. Evaluation of the feasibility of portal vein and superior mesenteric vein dissection is considered important.

  The anatomical specimen removed during pancreatoduodenal resection consists of the common bile duct, gallbladder, head, neck and secretory part of the pancreas, duodenum, proximal colon, small and part of the greater omentum, distal half of the stomach. In addition, paracaval tissue is subject to excision, suprapyloric, infrapiloric, anterior pancreatoduodenal, posterior pancreatoduodenal lymph nodes are removed. Lymph nodes of the hepatoduodenal ligament and along the common hepatic artery are also excised. The superior mesenteric vein is excised if it is isolated by a tumor, or the place of its confluence with the portal vein.

  The surgeon needs to perform a series of restorative procedures (pancreatojejunostomy, biliodigestive anastomosis, gastrojejunostomy and interintestinal anastomosis).

  Extended pancreatoduodenal resection involves the removal of the portal vein segment and arteries involved in the tumor process with vascular reconstruction. In addition, the retroperitoneal lymph nodes (from the celiac artery to the iliac bifurcation) are removed.

  The risk of death in the postoperative period is 5%. 5-year survival rates after pancreatoduodenal resections reach 20-25%, with an average survival rate of 8-11 months.

• Management of patients with pancreatic cancer

  Pancreatic cancer patients should be monitored by a gastroenterologist, oncologist, surgeon, and radiologist.

  • Only 15-20% of patients with pancreatic cancer are resectable. They undergo pancreatoduodenal resection (Whipple operation) followed by postoperative chemoradiation therapy.
  • About 30% of patients are diagnosed with unresectable locally advanced tumors without distant metastases. In these cases, chemotherapy and ionizing radiation are prescribed.
  • The neoadjuvant approach to the treatment of locally advanced pancreatic cancer can increase the percentage of resectable tumors and lengthen the life of patients.
  • Chemoradiotherapy can be used before surgery. In some cases, preoperative radiation therapy is performed followed by intraoperative radiation. This type of therapy increases patient survival to 2 years in 27% of cases; up to 5 years - in 7% of cases.
  • If the tumor is unresectable and jaundice is present, chemotherapy and palliative surgical procedures (endoscopic decompression with stenting) are performed.
  • In the presence of distant metastases, chemotherapy and palliative treatment are performed to relieve symptoms of the disease (pain).

13. Cardiogenic shock in myocardial infarction: pathogenesis, clinical picture, diagnosis, emergency care.

14. Heart rhythm disorders in myocardial infarction: prevention, treatment.

15. Pulmonary edema in myocardial infarction: clinical picture, diagnostics, emergency care.

16. Myocardial dystrophy: concept, clinical manifestations, diagnosis, treatment.

17. Neurocirculatory dystonia, etiology, pathogenesis, clinical variants, diagnostic criteria, treatment.

18. Myocarditis: classification, etiology, clinical picture, diagnosis, treatment.

19. Idiopathic diffuse myocarditis (Fiedler): clinical picture, diagnosis, treatment.

20. Hypertrophic cardiomyopathy: pathogenesis of intracardiac hemodynamic disorders, clinical picture, diagnosis, treatment. Indications for surgical treatment.

21. Dilated cardiomyopathy: etiology, clinical picture, diagnosis, treatment.

22. Pericardial effusion: etiology, clinical picture, diagnosis, treatment.

23. Diagnosis and treatment of chronic heart failure.

24. Insufficiency of the mitral valve: etiology, clinical picture, diagnosis, treatment.

25. Insufficiency of aortic valves: etiology, clinical picture, diagnosis, treatment.

26. Stenosis of the aortic mouth: etiology, clinical picture, diagnosis, treatment, indications for surgical treatment.

27. Stenosis of the left atrioventricular foramen: etiology, clinical picture, diagnosis, treatment. Indications for surgical treatment.

28. Ventricular septal defect: clinical picture, diagnosis, treatment.

29. Atrial septal overgrowth: diagnosis, treatment.

30. Patent ductus arteriosus (botalov): clinic, diagnostics, treatment.

31. Coarctation of the aorta: clinical presentation, diagnosis, treatment.

32. Diagnosis and treatment of dissecting aortic aneurysm.

33. Infective endocarditis: etiology, pathogenesis, clinical picture, diagnosis, treatment.

34. Syndrome of weakness of the sinus node, ventricular asystole: clinical manifestations, diagnosis, treatment.

35. Diagnosis and treatment of supraventricular paroxysmal tachycardia.

36. Diagnosis and treatment of ventricular paroxysmal tachycardia.

37. Clinical electrocardiographic diagnosis of III degree atrioventricular block. Treatment.

38. Clinical and electrocardiographic diagnostics of atrial fibrillation. Treatment.

39. Systemic lupus erythematosus: etiology, clinical picture, diagnosis, treatment.

40. Systemic scleroderma: etiology, pathogenesis, diagnostic criteria, treatment.

41. Dermatomyositis: diagnosis criteria, treatment.

42. Rheumatoid arthritis: etiology, clinical picture, diagnosis, treatment.

43. Deforming osteoarthritis: clinical picture, treatment.

44. Gout: etiology, pathogenesis, clinical picture, diagnosis, treatment.

Respiratory diseases

1. Pneumonia: etiology, pathogenesis, clinical picture.

2. Pneumonia: diagnosis, treatment.

3. Asthma: classification, clinical picture, diagnosis, treatment in the out-of-attack period.

4. Bronchoastmatic status: clinic by stage, diagnosis, emergency care.

5. Chronic obstructive pulmonary disease: concept, clinic, diagnosis, treatment.

6. Lung cancer: classification, clinical presentation, early diagnosis, treatment.

7. Lung abscess: etiology, pathogenesis, clinical picture, diagnosis.

8. Lung abscess: diagnosis, treatment, indications for surgery.

9. Bronchiectasis: etiology, pathogenesis, clinical picture, diagnosis, treatment, indications for surgery.

10. Dry pleurisy: etiology, clinical picture, diagnosis, treatment.

11. Exudative pleurisy: etiology, clinic, diagnosis, treatment.

12. Pulmonary embolism: etiology, main clinical manifestations, diagnosis, treatment.

13. Acute cor pulmonale: etiology, clinical picture, diagnosis, treatment.

14. Chronic cor pulmonale: etiology, clinical picture, diagnosis, treatment.

15. Relief of status asthmaticus.

16. Laboratory and instrumental diagnostics of pneumonia.

Diseases of the gastrointestinal tract, liver, pancreas

1. Peptic ulcer and 12 duodenal ulcer: clinical picture, differential diagnosis, complications.

2. Treatment of peptic ulcer disease. Indications for surgery.

3. Diagnostics and treatment tactics for gastrointestinal bleeding.

4. Stomach cancer: clinical presentation, early diagnosis, treatment.

5. Diseases of the operated stomach: clinical picture, diagnostics, possibilities of conservative therapy.

6. Irritable bowel syndrome: modern concepts of pathogenesis, clinical picture, diagnosis, treatment.

7. Chronic enteritis and colitis: clinical picture, diagnosis, treatment.

8. Ulcerative colitis, Crohn's disease: clinical picture, diagnosis, treatment.

9. Colon cancer: dependence of clinical manifestations on localization, diagnosis, treatment.

10. The concept of "acute abdomen": etiology, clinical picture, tactics of the therapist.

11. Biliary dyskinesia: diagnosis, treatment.

12. Cholelithiasis: etiology, clinical picture, diagnostics, indications for surgical treatment.

13. Diagnostic and therapeutic tactics for biliary colic.

14 .. Chronic hepatitis: classification, diagnosis.

15. Chronic viral hepatitis: clinical picture, diagnosis, treatment.

16. Classification of liver cirrhosis, the main clinical and paraclinical syndromes of cirrhosis.

17. Diagnostics and treatment of liver cirrhosis.

18 Biliary cirrhosis of the liver: etiology, pathogenesis, clinical and paraclinical syndromes, diagnosis, treatment.

19. Liver cancer: clinical picture, early diagnosis, modern methods of treatment.

20. Chronic pancreatitis: clinical picture, diagnosis, treatment.

21. Pancreatic cancer: clinical picture, diagnosis, treatment.

22. Chronic viral hepatitis: diagnosis, treatment.

Kidney disease

1. Acute glomerulonephritis: etiology, pathogenesis, clinical variants, diagnosis, treatment.

2. Chronic glomerulonephritis: clinical picture, diagnosis, complications, treatment.

3. Nephrotic syndrome: etiology, clinical picture, diagnosis, treatment.

4. Chronic pyelonephritis: etiology, clinical picture, diagnosis, treatment.

5. Diagnostic and therapeutic tactics for renal colic.

6. Acute renal failure: etiology, clinical picture, diagnosis, treatment.

7. Chronic renal failure: clinical picture, diagnosis, treatment.

8. Acute glomerulonephritis: classification, diagnosis, treatment.

9. Modern methods of treatment of chronic renal failure.

10. Causes and treatment of acute renal failure.

Blood diseases, vasculitis

1. Iron deficiency anemia: etiology, clinical picture, diagnosis, treatment

2. B12-deficiency anemia: etiology, pathogenesis, clinic

3. Aplastic anemia: etiology, clinical syndromes, diagnosis, complications

4 Hemolytic anemia: etiology, classification, clinical picture and diagnosis, treatment of autoimmune anemia.

5. Congenital hemolytic anemias: clinical syndromes, diagnosis, treatment.

6. Acute leukemia: classification, clinical picture of acute myeloblastic leukemia, diagnosis, treatment.

7. Chronic lymphocytic leukemia: clinical picture, diagnosis, treatment.

8. Chronic myeloid leukemia: clinical picture, diagnosis, treatment

9. Lymphogranulomatosis: etiology, clinical picture, diagnosis, treatment

10. Erythremia and symptomatic erythrocytosis: etiology, classification, diagnosis.

11. Thrombocytopenic purpura: clinical syndromes, diagnosis.

12. Hemophilia: etiology, clinic, treatment.

13. Diagnostic and treatment tactics for hemophilia

14. Hemorrhagic vasculitis (Shenlein-Henoch disease): Clinical picture, diagnosis, treatment.

15. Thromboangiitis obliterans (Winivarter-Buerger disease): etiology, clinical picture, diagnosis, treatment.

16. Nonspecific aortoarteritis (Takayasu's disease): options, clinical picture, diagnosis, treatment.

17. Polyarteritis nodosa: etiology, clinic, diagnosis, treatment.

18. Wegener's granulomatosis: etiology, clinical syndromes, diagnosis, treatment.

Endocrine system diseases

1. Diabetes mellitus: etiology, classification.

2. Diabetes mellitus: clinic, diagnostics, treatment.

3. Diagnosis and emergency treatment of hypoglycemic coma

4. Diagnosis and emergency treatment of ketoacidotic coma.

5. Diffuse toxic goiter (thyrotoxicosis): etiology, clinical picture, diagnosis, treatment, indications for surgery.

6. Diagnostics and emergency treatment of thyrotoxic crisis.

7. Hypothyroidism: clinical picture, diagnosis, treatment.

8. Diabetes insipidus: etiology, clinical picture, diagnosis, treatment.

9. Acromegaly: etiology, clinical picture, diagnosis, treatment.

10. Itsenko-Cushing's disease: etiology, clinical picture, diagnosis, treatment.

11. Obesity: etiology, pathogenesis, clinical picture, diagnosis, treatment.

12. Acute adrenal insufficiency: etiology, course options, diagnosis, treatment. Waterhouse-Friederiksen syndrome.

13. Chronic adrenal insufficiency: etiology, pathogenesis, clinical syndromes, diagnosis, treatment.

14. Treatment of type 2 diabetes.

15. Relief of the crisis with pheochromocytoma.

Occupational pathology

1. Occupational asthma: etiology, clinic, treatment.

2. Dust bronchitis: clinical picture, diagnosis, complications, treatment, prevention.

3. Pneumoconiosis: clinical picture, diagnosis, treatment, prevention

4. Silicosis: classification, clinical picture, treatment, complications, prevention.

5. Vibration disease: forms, stages, treatment.

6. Intoxication with organophosphate insectofungicides: clinic, treatment.

7. Antidote therapy for acute occupational intoxication.

8. Chronic lead intoxication: clinical picture, diagnosis, prevention, treatment.

9. Occupational asthma: etiology, clinic, treatment.

10. Dust bronchitis: clinical picture, diagnosis, complications, treatment, prevention.

11. Poisoning with organochlorine pesticides: clinical picture, diagnosis, treatment, prevention.

12. Features of the diagnosis of occupational diseases.

13. Intoxication with benzene: clinical picture, diagnosis, treatment, prevention.

15. Poisoning with organophosphorus compounds: clinical picture, diagnostics, prevention, treatment.

16. Intoxication with carbon monoxide: clinical picture, diagnosis, treatment, prevention.

21. Pancreatic cancer: clinical picture, diagnosis, treatment.

Pancreatic cancer is a group of primary malignant tumors that are localized in the ducts and acini of the pancreas.

These tumors include: ductal adenocarcinomas, giant cell adenocarcinomas, mucinous adenocarcinomas, mucinous cystadenocarcinomas, glandular squamous cell carcinoma, acinar carcinoma, pancreatoblastomas, intraductal papillary mucoid tumors.

the initial symptoms of pancreatic cancer (weight loss, weakness, fatigue, abdominal pain, nausea, vomiting, anorexia) are nonspecific. As the disease progresses, the symptoms become more pronounced.

The main manifestations of pancreatic cancer

Stomach ache.

As the tumor grows, the pain in the abdomen becomes intense, sharp, radiating to the back and intensifying when the body bends forward. Irradiation of back pain indicates a tumor affecting the retroperitoneal region.

When the tumor is localized in the tail of the pancreas, pain is recorded in 87% of patients, with head cancer - in 72% of patients.

Adenocarcinomas localized in the head of the pancreas, in 80-90% of cases, lead to jaundice (as a result of compression of the common bile duct by a tumor). Itching, darkening of urine and lightening of feces are also noted.

Weight loss.

This symptom is observed in 92% of patients with tumor localization in the head and in 100% of patients with damage to the body or tail of the pancreas. Weight loss may be associated with steatorrhea (as a result of impaired exocrine pancreatic function).

Anorexia.

Nausea and vomiting.

Nausea and vomiting are noted in 43-45% of cases with head cancer and in 37% of cases with tail and body cancer. These symptoms may be the result of compression of the duodenum and stomach by a tumor.

Development of secondary diabetes mellitus.

Diabetes mellitus as a consequence of cancer is diagnosed in 25-50% of patients, leading to the appearance of symptoms such as polyuria and polydipsia.

If the tumor is located in the body or in the tail of the pancreas, then it contributes to the occurrence of splenomegaly, bleeding from varicose veins of the esophagus and stomach.

In some cases, a clinical picture of acute cholecystitis or acute pancreatitis develops.

Peritoneal metastases can cause intestinal compression with symptoms of constipation or obstruction.

It is difficult to suspect the presence of pancreatic cancer in the early stages of development, since the clinical manifestations of the disease are nonspecific. Pancreatic cancer is difficult to diagnose at an early stage. Only 30% of patients are diagnosed within 2 months. after the onset of the disease. This is due to the fact that the initial symptoms of pancreatic cancer (weight loss, weakness, fatigue, abdominal pain, nausea, vomiting, anorexia) are nonspecific. Therefore, timely treatment of patients with doctors and a full examination is of paramount importance.

Pancreatic cancer can be suspected when jaundice appears and the intensity of abdominal pain increases.

Diagnostic goals

Identify pancreatic cancer.

Install its localization.

Identify metastases.

Establish the stage of the cancer.

Establish tumor resectability or unresectability.

Diagnostic methods

Taking anamnesis

As the disease progresses, the initial symptoms (weight loss, weakness, fatigue, abdominal pain, nausea, vomiting, anorexia) become more pronounced.

When taking anamnesis, it is important to assess the place and impact of various risk factors on patients' lives.

Smoking can be the cause of pancreatic cancer in 30% of cases.

The disease is more common in people who consume foods high in carbohydrates.

In patients with type I or II diabetes for 5 years or more, the risk of pancreatic cancer is doubled.

In about 5-10% of patients, the occurrence of pancreatic cancer is the result of hereditary pathology. Thus, this disease is diagnosed in patients with hereditary non-polyposis colorectal cancer, ataxia-telangiectasia, hereditary pancreatitis, familial adenomatous polyposis, Gardner's and Gippel-Landau's syndromes, with BRCA2 gene mutations.

Chronic pancreatitis is a risk factor for pancreatic cancer in 5% of patients.

Gastrectomy and gastric resection performed in patients with peptic ulcers, benign stomach tumors, increase the risk of developing pancreatic cancer by 3-5 times.

Physical examination

Abdominal pain is the main symptom of pancreatic cancer. When the tumor is localized in the tail of the pancreas, they are recorded in 87% of patients, with head cancer - in 72% of patients. As the disease progresses, abdominal pains become intense, sharp, radiate to the back and intensify when the body bends forward. Irradiation of back pain indicates a tumor affecting the retroperitoneal region.

Adenocarcinomas localized in the head of the pancreas, in 80-90% of cases, lead to jaundice (as a result of compression of the common bile duct by a tumor). Therefore, patients complain of itchy skin, darkening of urine and lightening of feces. On the skin of patients, you can find traces of scratching (due to pronounced itching).

Weight loss is observed in 92% of patients with tumor localization in the head and in 100% of patients with lesions of the body or tail of the pancreas.

Anorexia is observed in 64% of patients with head cancer and in about 30% of patients with tumor localization in other parts of the pancreas.

Nausea and vomiting are observed in 43-45% of cases with head cancer and 37% for tail and body cancer.

Diabetes mellitus as a consequence of cancer is diagnosed in 25-50% of patients, leading to the appearance of symptoms such as polyuria and polydipsia. However, only in 1% of patients with newly diagnosed diabetes mellitus, it is possible to establish a connection between this disease and pancreatic cancer.

In some cases, a clinical picture of acute cholecystitis or acute pancreatitis develops (in 5% of patients).

Physical examination of patients with pancreatic cancer may reveal tension in the peri-epigastric region on palpation.

In 50% of patients with jaundice (with cancer of the head of the pancreas), Courvoisier's symptom can be detected (a distended gallbladder is palpable).

If the tumor is located in the body or in the tail of the pancreas, then it contributes to the occurrence of splenomegaly, bleeding from varicose veins of the esophagus and stomach.

At a late stage of the disease, ascites and hepatomegaly develop.

In some cases, deep vein thrombosis, thrombophlebitis are noted.

Metastases in the peritoneum can lead to intestinal compression with symptoms of constipation or obstruction.

Almost 67% of patients are severely depressed.

Laboratory diagnostic methods

General blood analysis

A general blood test may reveal normochromic anemia, an increase in the number of platelets. An acceleration of ESR is observed.

Blood chemistry

The results are most often nonspecific.

An increase in the content of bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase, ALT, ASAT is noted, which may indicate obstruction of the bile ducts or cancer metastases to the liver.

In the blood of patients with pancreatic cancer with compression of the bile duct, bilirubin values \u200b\u200bdaily increase by 3 mg / dL (51.3 mmol / L), and in total duct obstruction by 12-16 mg / dL (205.2-273.6 mmol / l).

Amylase and lipase, pancreatic ribonuclease, elastase, trypsin inhibitors may increase.

An increase in C-reactive protein values \u200b\u200bcan be detected.

Due to the development of malabsorption syndrome, the levels of albumin and cholesterol decrease.

Determination of pancreatic cancer markers

Marker CA-19-9.

It is produced by cells of the pancreatic ducts, cells of the liver and bile ducts. It is found in 5-10% of healthy people. It is found in 75-85% of patients with pancreatic cancer. However, it is not specific for this disease, as it increases in liver cancer (in 67% of cases), stomach cancer (in 62% of cases), and colon cancer (in 19% of cases).

The level of CA-19-9 increases with the progression of the disease (37 U / ml - the upper limit of the norm). If its indicators are higher than 100 U / ml, then this is evidence in favor of a malignant process. The marker exceeds the reference values \u200b\u200bfor tumors larger than 3 cm. If the CA-19-9 level is more than 1000 U / ml, then the tumor is larger than 5 cm.

Determination of this marker is important for resolving the issue of tumor resectability. Less than 4% of patients with CA-19-9 levels greater than 300 U / ml have resectable tumors.

However, the definition of CA-19-9 cannot serve as a screening method, since using this method it is impossible to detect pancreatic cancer in the early stages.

Instrumental diagnostic methods

Transabdominal ultrasonography - abdominal ultrasound

Allows to exclude gallstone disease in patients with jaundice and pain syndrome. In about 30% of cases, the pancreas is not visualized (due to ascites, flatulence, obesity).

Ultrasound can detect the expansion of the pancreatic ducts; compression of the common bile duct by a tumor, cancer metastases to the liver. An increase in the head of the pancreas to 2.6 cm suggests cancer.

Endoscopic ultrasonography

Allows to detect pancreatic carcinomas in 99-100% of cases. The accuracy of this method for assessing cancer staging is 70-80%. This study allows you to assess the condition of the portal and superior mesenteric veins, as well as visualize metastases to regional lymph nodes or celiac trunk.

During the implementation of the method, an aspiration biopsy of the tumor and metastatic lymph nodes can be performed.

Computed tomography (CT)

Allows to identify tumor lesions of the pancreas and the state of the hepatobiliary zone; germination of the tumor of the superior mesenteric vessels, metastases of cancer to the liver and other organs, expansion of the pancreatic duct distal to the tumor. In addition, using this method, you can clarify the stage of the disease. Tumors larger than 1 cm are visualized.

The sensitivity of the method is 90%; specificity 80%.

With the help of CT, the tumor resectability can be estimated at 72%; unresectability in 100% of cases. If the tumor is no more than 2-3 cm in size on CT and there is no vascular involvement, then it is resectable.

Magnetic resonance imaging (MRI)

Allows to detect tumors less than 2 cm in size. In patients with jaundice, it is used to assess the state of the biliary tract and pancreatic duct.

Positron emission tomography

Allows you to identify primary tumors and metastases. False positive results can be obtained in patients with pancreatitis.

Transhepatic cholangioangiography

This test can identify the tumor and detect compression of the superior mesenteric vein or portal vein.

Retrograde endoscopic cholangiopancreatography

It has a high diagnostic value. This study allows you to detect tumors in the pancreas (up to 2 cm) in any part of it. Using the method, you can assess the composition of the pancreatic secretion.

If during the study, pancreatic ducts of irregular shape, ending in narrowing, are visualized, then the probability of ductal cancer is high (more than 90%).

Complications during this procedure are observed in 5-10% of cases.

Laparoscopy

Laparoscopy detects small metastases of cancer to the liver and peritoneum. You can also get ascitic fluid for subsequent cytological examination.

There is also a method of laparoscopic ultrasound, which can detect small metastases in the liver, more accurately staging pancreatic cancer.

Aspiration biopsy

Performed during endoscopic ultrasonography in the preoperative period. The need for this procedure is debated, since the probability of tumor cell dissemination is high. If the method is performed under CT control, then it is possible to reduce possible risks.

Cytological examination of the obtained tissue samples allows diagnosing pancreatic cancer in 85-95% of cases. Ductal adenocarcinomas are found in more than 80% of patients.

Treatment goals

Removal of the tumor in case of resectability (pancreatoduodenal resection is performed - Whipple operation).

Increase in the percentage of resectable tumors by restaging.

Reducing the severity of clinical manifestations of cancer (relief of pain syndrome, decrease in the severity of jaundice, correction of disorders of the exocrine function of the pancreas).

Increased survival rates.

Treatment methods

Diet therapy

Most patients with pancreatic cancer have anorexia. They also develop malabsorption syndrome due to impaired exocrine pancreatic function. Therefore, foods high in fat and protein should be excluded from the diet of these patients. Read more: Nutritional therapy for cancer.

Medication methods of treatment

Chemotherapy of disseminated pancreatic cancer in monotherapy regimen

Fluorouracil.

Fluorouracil (FU) is a synthetic analogue of the naturally occurring pyrimidine - uracil. The main target is the enzyme thymidylate synthetase, which controls the synthesis of normal thymidine nucleotides. During infusion, the Fluorouracil solution must be protected from light. Patients are advised not to use aspirin and other non-steroidal anti-inflammatory drugs together with Fluorouracil.

The drug is used in different modes:

500 mg / m 2 IV stream for 5 consecutive days, every 4 weeks or

500-600 mg / m 2 IV, jet once a week, 6 weeks or

1000 mg / m 2 IV, infusion for 5 days (120 hours) every 4 weeks or

200-300 mg / m 2 IV, by infusion for a month or

2.6 g / m 2 IV, infusion over 24 hours, once a week, 4-5 weeks.

Mitomycin C (MMS).

MMS is an antibiotic in origin, according to the mechanism of action it refers to alkylating agents that require activation in vivo. The side effects of MMS include leukopenia and especially thrombocytopenia. Rarely, the drug causes the development of interstitial pneumonia, when used together with anthracyclines, it increases the cardiotoxicity of the latter.

The drug is administered intravenously. It is prescribed at 10-20 mg / m 2 every 6-8 weeks, or 5-6 mg / m 2 every 4 weeks.

Ifosfamide (IFO).

Refers to chloroethylamines, is a synthetic analogue of cyclophosphamide. It is activated in the liver by microsomal enzymes. Its active metabolite, 4-hydroxyphosphamide, alkylates DNA, causing it to break, as well as RNA, and inhibits protein synthesis.

Complications are observed: myelosuppression, nausea, vomiting, diarrhea and sometimes constipation, alopecia, hepatotoxicity, rarely lethargy, hallucinations; symptoms of cystitis may occur - dysuria, frequent urination.

The most common modes (I / O):

1000 mg / m 2 5 consecutive days every 3 weeks or

1.2-2.4 g / m2 3 consecutive days every 3 weeks or

5000 mg / m 2 once every 3 weeks.

Radiation therapy

Treatment is carried out preoperatively, intraoperatively, postoperatively, in combination with chemotherapy.

Radiation therapy for patients with pancreatic cancer uses different doses of radiation.

For palliative purposes (pain control, jaundice, prevention of bleeding), the radiation dose is 50 Gy. Higher doses of more than 60 Gy are prescribed to patients in order to improve survival rates.

Preoperative radiation is rarely used.

Intraoperative radiation can be combined with external radiation in order to increase the dose to the pancreas and provide better local control of the disease. The intraoperative radiation dose varies from 10 to 20 Gy; external - from 45 to 50 Gy. Remission within a year is observed in 82% of patients.

Surgery

Surgical treatment is performed in the absence of distant metastases and radiographic or clinical signs of tumor unresectability.

Preoperative concepts of tumor resectability are preliminary. The final decision is made after an intraoperative examination of the abdominal organs (liver, peritoneum, periaortic and celiac lymph nodes) to exclude distant metastases. Then the possibilities of local tumor resectability are determined.

Pancreatoduodenal resection (Whipple operation) is the main type of radical surgery. It is not performed if the tumor invades the inferior vena cava, aorta, superior mesenteric artery, superior mesenteric vein, portal vein. To decide on the operation, it is necessary to mobilize the duodenum and the head of the pancreas from the underlying inferior vena cava and aorta. This technique also allows one to judge the involvement of the superior mesenteric artery. Evaluation of the feasibility of portal vein and superior mesenteric vein dissection is considered important.

The anatomical specimen removed during pancreatoduodenal resection consists of the common bile duct, gallbladder, head, neck and secretory part of the pancreas, duodenum, proximal colon, small and part of the greater omentum, distal half of the stomach. In addition, paracaval tissue is subject to excision, suprapyloric, infrapiloric, anterior pancreatoduodenal, posterior pancreatoduodenal lymph nodes are removed. Lymph nodes of the hepatoduodenal ligament and along the common hepatic artery are also excised. The superior mesenteric vein is excised if it is isolated by a tumor, or the place of its confluence with the portal vein.

The surgeon needs to perform a series of restorative procedures (pancreatojejunostomy, biliodigestive anastomosis, gastrojejunostomy and interintestinal anastomosis).

Extended pancreatoduodenal resection involves the removal of the portal vein segment and arteries involved in the tumor process with vascular reconstruction. In addition, the retroperitoneal lymph nodes (from the celiac artery to the iliac bifurcation) are removed.

The risk of death in the postoperative period is 5%. 5-year survival rates after pancreatoduodenal resections reach 20-25%, with an average survival rate of 8-11 months.

The main factors in the etiology of pancreatic cancer are smoking, alcohol, unhealthy diet, occupational hazards, drugs, heredity,.

Smoking

When smoking, the risk of developing the disease increases 3 times. In 1986, the International Agency for Research on Cancer classified smoking as a carcinogenic factor that significantly increases the likelihood of pancreatic cancer. Research indicates a dose-dependent relationship that requires long-term exposure.

It is not known what kind of carcinogen acts in the composition of cigarette smoke. The time during which cigarette smoke begins to have its negative impact is also discussed. Some studies indicate that the disease occurs with a smoking experience of 15 years.

Alcohol

The role of alcohol in the etiology of pancreatic cancer is controversial. An association has been reported in two case-control studies. Other authors do not confirm this pattern. In the analysis prior to these studies, the IARC Working Group excluded alcohol from the risk factors.

Food

Through detailed cohort analysis and case-control studies, basic information has been obtained about the effect of dietary habits on cancer development. Indicate the significant role of a diet high in fat. However, these data are not entirely reliable. Total energy consumption also plays a role. Influence energy value the diet is possibly exaggerated; an increase in body mass index introduces a certain uncertainty. The relative risk for obesity is 1.72. It has been suggested that growth also increases the risk of illness, although this may be due to the use of surrogate products in childhood. Vitamin C and fiber have a protective effect. The caffeine intake contributes to the etiology of pancreatic cancer. The significance of all these factors is highly controversial, and their role is minimized.

Occupation

The risk of developing adenocarcinoma of the pancreas is slightly higher in workers exposed to ionizing radiation or in contact with aluminum, acrylamide and halogenated hydrocarbons. In particular, work involving dry cleaning carries a comparative risk of 1.5. These data are generally inconclusive; the correlation between occupational activity and cancer occurrence is controversial.

Prior use of medications

The greatest interest is given to patients with diabetes. The risk is especially high immediately after diagnosis. Whether these conditions are based on similar causes, whether pancreatitis and diabetes are precursors of cancer or are directly involved in carcinogenesis, has not been established. When chronic pancreatitis the risk of developing cancer approaches normal after 10 years; in diabetes, the positive relationship persists for more than 5 years. Gardner's syndrome and multiple endocrine neoplasia type 1 (neuroendocrine cancer) are also associated with pancreatic cancer.

Hereditary pancreatic cancer

The true prevalence of pancreatic cancer has only recently become clear. Previously, despite various reports of familial cases, it was believed that there was a significant familial predisposition to the disease. D.T. Silverman has shown a significant increase in the risk of pancreatic cancer among individuals in whom first-degree relatives have had cancer, especially when combined with smoking. This was confirmed in a cohort study, when the probability coefficient among relatives of the first degree of relationship was equal to 1.5. 7% of cases of etiology of pancreatic cancer are due to genetic factors. Known familial diseases, such as those with the STK11 / LKB1 gene, BRCA2 expression, and multiple atypical nevi syndrome (the p16 gene is inactivated in 95% of sporadic cancers), may predispose to the etiology of pancreatic cancer. An association with familial adenomatous polyposis, carriage of the BRCA1 gene and von Hippel-Lindau disease is also indicated, but an increase in risk has not been confirmed.

Precancerous conditions

Determining antecedent conditions and identifying factors that play a role in the etiology of pancreatic cancer are difficult, in part due to the lack of an accurate animal model of the disease. Despite this drawback, the molecular pathways by which the formation of the neoplastic phenotype occurs are currently well understood. The introduction of the analysis of the genetic microarray of normal and pathologically altered pancreatic tissue into practice is a major breakthrough not only in terms of diagnostic efficiency, but also in identifying new areas of research. The p16 tumor suppressor gene is important, as its function is lost in 95% of cancers. This is usually due to homozygous deletion, loss of heterozygosity, or promoter methylation. Sometimes, p16 inactivation can be a hereditary defect. The K-ras gene mediates signaling of growth factor receptors, and its mutations are found in more than 90% of cases of duct damage. Dysregulation of the cell cycle (especially inhibition of the transition to the S phase and the loss of the protein p53 mediating it) is detected in 50% of patients with pancreatic cancer. Other targets are the transforming growth factor b gene receptor, the BRCA2, HER-2 / NEU, DPC4, MKK4 and EBER-1 genes.

Johns Hopkins University recently suggested that intraepithelial neoplasia (PanIN stands for pancreatic intraepithelial neoplasms) is a precursor to invasive pancreatic cancer. The model is similar to that in carcinoma in situ of the duct of the breast or adenomatous polyp in colon cancer. According to this model, an atypical mucus-forming epithelium replaces the physiological cuboid. Evidence that PanIN is indeed a precancerous condition depends on the circumstances, although it can be questioned. These lesions were initially detected more often during resection of adenocarcinoma than in the tissues of the pancreas not affected by the neoplasm. The more atypical PanIN-2 and PanIN-3 are found in the pancreas exclusively in the presence of cancer. The proportion of p16 and K-ras mutations increases in parallel with an increase in PanIN atypicality. These data make it possible to form a model of oncogenesis with a sequential progression of PanIN (1A) to invasive adenocarcinoma. Like carcinoma in situ in the ducts of the breast, the natural development and course of the process remains to be elucidated.

The article was prepared and edited by: surgeon

The content of the article

Pancreas cancer currently makes up an insignificant share in the total structure of oncopathology, equal to 2% of all malignant tumors. There is a steady increase in morbidity and mortality from this pathology throughout the world. Men get sick 2.5 times more often than women.

Pancreatic cancer etiology

Pancreas cancer - polyetiological disease. A certain role in the development of this pathology is assigned to nutritional factors ( western diet), bad habits (alcohol abuse, smoking), chronic inflammatory processes in the pancreas. The most common tumor localization in pancreatic cancer is the head (up to 70% of all cases), the body (20%), the tail (0.5%); and total lesion of the gland occurs in 5% of cases.

Pathological anatomy of pancreatic cancer

The tumor develops from the glandular elements, the epithelium of the excretory ducts and from the pancreatic islets of Langerhans. According to the histological structure, adenocarcinoma, solid cancer, undifferentiated and unclassified cancer are distinguished. The spread of the tumor occurs by the lymphogenous and hematogenous pathways. Pancreatic and pancreatoduodenal lymph nodes are most often affected. Distant metastases are found in the lungs, liver, bones, peritoneum.

Pancreatic Cancer Clinic

The clinical picture of pancreatic cancer consists of symptoms caused by the tumor itself, and symptoms associated with complications of tumor growth. For the first group, pain in the epigastric region, weakness, weight loss, and anorexia are most characteristic. Another group of signs is a consequence of obstruction of the pancreatic ducts (pain, intestinal disorders, secondary diabetes) and extrahepatic (jaundice, pruritus, enlargement of the liver and gallbladder, fever) of the bile ducts, as well as a consequence of obturation of the duodenal lumen (heaviness in the epigastric region, vomiting, etc., i.e., the clinic of stenosis of the anthrapoid stomach). It is rarely possible to palpate the tumor.

Pancreatic Cancer Diagnosis

The diagnosis of pancreatic cancer is complex and usually requires an integrated approach. The diagnosis is made on the basis of clinical and anamnestic data, results of laboratory, X-ray, endoscopic, radionuclide research methods. IN recent times in the diagnosis of pancreatic tumors, ultrasound scanners and computed tomography, angiography are used. The reliability of the above research methods varies widely, therefore the final diagnosis can be established only on the basis of histological examination data.

Pancreatic cancer classification

TNM classification
pT - primary tumor:
pT 0 - the primary tumor is not detected;
pT 1 - the tumor is limited to the pancreas, has a diameter of 2-3 cm;
pT 2 - the tumor has spread to any of the following structures: duodenum, bile duct;
pT 3 - the tumor spreads to any of the following structures: stomach, spleen, colon, adjacent great vessels;
pT X - insufficient data to assess the primary tumor.
N - regional lymph nodes:
N 0 - no signs of metastatic lesions of regional lymph nodes;
N 1 - metastases in regional lymph nodes;
N X - insufficient data to assess regional lymph nodes.
M - distant metastases:
M 0 - no signs of distant metastases;
M 1 - there are distant metastases;
M X - insufficient data to assess distant metastases.
G - pathological differentiation:
G 1 - high degree of differentiation;
G 2 - the average degree of differentiation;
G 3 - low degree of differentiation;
G 4 - undifferentiated tumor;
G X - the degree of differentiation is not determined.
Grouping by stage:
stage I - T 1 N 0 M 0, T 2 N 0 M 0;
stage II - T 3 N 0 M 0;
stage III - any category T, N1 M0;
stage IV - any category T, any category N M 1.